Bleeding Brain Intraparenchymal

International Journal of Trend in Scientific Research and Development (IJTSRD)
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Bleeding Brain Intraparenchymal
Renato Serquiz E Pinheiro¹, Yanny Cinara T Ernesto2, Irami Araújo-Neto2,
Fausto Pierdoná Guzen3, Amália Cinthia Meneses Rêgo3, Irami Araújo-Filho3,4
1Professor of the Medicine Course of the Potiguar University - UnP, Natal, Brazil
2Student of the Medicine Course of the Potiguar University - UnP, Natal, Brazil
3Graduate Program in Biotechnology of the University Potiguar - UnP, Natal, Brazil
4Associate Professor II, Department of Surgery – UFRN, Natal, Brazil
How to cite this paper: Renato Serquiz
E Pinheiro | Yanny Cinara T Ernesto |
Irami Araújo-Neto | Fausto Pierdoná
Guzen | Amália Cinthia Meneses Do
Rêgo | Irami Araújo-Filho "Bleeding
Brain Intraparenchymal" Published in
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ABSTRACT
Despite the diagnostic and therapeuticadvances,intraparenchymalhemorrhage
(HIP) continues to present high Indices of mortality and disability. Its clinical
differentiation with ischemic stroke from neuroimaging examination is
fundamental. There is no specific treatment for a HIP. Its management consists
of support and approach measures on intracranialhypertension,beingreserved
for the intervention Surgical in selected cases. Minimally invasive surgical
techniques are underway. This study aims to reviewand discusstheapproach of
intraparenchymatous hemorrhages in medical practice.
KEYWORDS: brain hemorrhage, brain parenchymal hemorrhage, brain
hemorrhage, cerebrovascular accident, cerebrovascular stroke, brain vascular
accident.
INTRODUCTION
According to the Brazilian Society of Cerebrovascular
Diseases, hemorrhagic stroke is the whole event caused by
spontaneous (non-traumatic) rupture of a vessel, with
extravasation of blood tothe insideofthebrain(hemorrhage
intraparenchymal), for the ventricular system
(intraventricular hemorrhage) and/or subarachnoid space
(subarachnoid hemorrhage)1.
Intraparenchymal hemorrhage (HIP) is a common disease,
responsible for 10-20% of cerebrovascular accidents. It is
more incident with the increase of age, doubling every ten
years after the 35 years, in males and influenced by racial
factors, being more frequent In Afro, Hispanic, Latin and
Asian when compared to the Caucasian population2,3. In
general, 30-day mortality of these patients is up to
approximately 45% and mortality in 1 year is about 63%4,5.
Methods
This Is the literature review study, whose bibliographic
research was carried out in Pubmed, Scopus, Scielo and
Uptodate Databases. The descriptors used “brain
hemorrhage”, “brain parenchymal hemorrhage”, “brain
hemorrhage”, “cerebrovascular accident”, “cerebrovascular
stroke”, “brain vascularaccident”.Theinclusion criteria,were
selected articles published in English, Spanish and
Portuguese; Randomized Clinical Trials / Clinical Trial),
Guidelines (Guideline), Systematic Reviews, Reviews and
Meta-Analysis. The selection of articles was made by listing
those of greater relevance according to the proposed theme,
both In the foreign and Brazilian literature, in a non-
systematic way, addressing from itsetiologytothedefinitive
treatment.
Etiology
The spontaneous HIP may be classified as primary or
secondary depending on the underlying cause6-8:
Primary: It represents about 80-85% of cases and
occurs due to spontaneous rupture of small vessels
damaged by uncontrolled chronic hypertension or
angiopathy amyloid (AAC), causing the so-called
aneurysms of Charcot-Bouchard. It is alsodifferentiated
as to the location in Lobar (commonly resulting from
AAC) and not Lobar (often due to long-standing arterial
hypertension) and, in the latter, Putamen, Thalamus,
subcortical white matter, bridge and cerebellum, the
most common sites.
IJTSRD23500

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Secondary: Corresponds to 15-25% of cases and is
associated with a series of congenital and acquired
conditions, such as vascular pathologies (arteriovenous
malformations, Moyamoya, Cavernomas, Venous
Angiomas and Telangiectasis), tumors, hemorrhagic
transformation of cerebral ischemia, leukemia,
coagulation disorders, use of anticoagulants and
thrombolytic agents, cerebral vasculitis, drug abuse,
cerebral venous thrombosis, among other causes.
Risk Factors
Non-modifiable
Advanced age;
Black and Oriental breed;
Male.
Modifiable
Hypertension: is the main risk factor, being present in
70 to 80% of patients with HIP;
Angiopathy Amyloid: is characterized by deposits of
the beta peptide Amyloid within small and medium
vessels of the cortex and leptomeningeal.Itmayoccur as
a sporadic disorder, sometimes in association with
Alzheimer's disease, or asaspecificfamilialsyndrome.It
is a significant cause of HIP lobar primary in the elderly,
especially in the parietal and occipital lobes;
Smoking: Smokers have a higher risk of stroke,
including HIP than in non-smokers;
Alcohol: Consumption of moderate or large quantities
of alcohol in the 24h preceding the ictus seems to
precipitate HIP;
Coagulopathies: Both the coagulopathies primary and
secondary, such as the use of oral anticoagulants,
antiplatelet drugs, thrombolytics for the treatment of
acute ischemic stroke or acute myocardial infarction
(AMI) are associated with increased risk of the HIP;
Sympathomimetics Medicines or drugs with
sympathomimetic activity, (Phenylpropanolamine,
cocaine, amphetamines, or ephedrine) also increasethe
risk of the HIP;
Cholesterol and triglyceride Status: There may be an
inverse relationship between the levels of total
cholesterol, LDL and triglycerides and the risk of a HIP.
Other: Less established factors, such as obesity and
genetic factors, are also pointed out as relevant to the
risk of the HIP.
Clinical picture
HIP is usually characterized by thesuddenfocalneurological
deficit, dependent on the bleedingtopography,suddenonset
and rapidly progressive. Although frequent, the headache is
not present in all cases, only when the HIP is accompanies of
meningeal irritation due to intraventricular hemorrhage or
subarachnoid associated,orincreased intracranial pressure9.
For this last reason or by distortion of brain structures, the
vomiting is associated. Convulsive seizures may occur,
especially in bleeding Lobar10.
Bleeding in the Putamen occurs in approximately35%ofthe
cases, subcortical in 30%, cerebellum in 16%, thalamus in
15% and bridge in 5-12%11-13. They manifest themselves
with:
Putamen: Hemiplegia, loss hemisensory, hemianopsia
homonymous, gaze paralysis, torpor, and coma.
Cerebellar: Imbalance, vomiting, headache (usually
occipital), stiffness nuchal, paralysis of the gaze, facial
paresis or even torpor due to compression of the
brainstem. It is a crucial diagnosis since these patients
frequently deteriorate and require surgery.
Thalamic: hemiparesis, loss hemisensory and
occasionally hemianopsia transient homonymous, and
there may be pupils miotic non-reactive. Aphasia can
occur if bleeding affects the dominant hemisphere or
neglect in the non-dominant hemisphere.
Pontina: Usually leads to deep coma in the first few
minutes after hemorrhage, probably due to rupture of
the reticular activation system. The motor examination
is marked by total paralysis. The pupils are reactive, but
the ocular movements are absent, and there may be
ocular oscillation, facial paralysis, deafness, and
dysarthria. When the patient is awake.
It is also essential that all patients with suspected HIP are
evaluated by the Glasgow Coma Scale and by NIHSS
(National Institutes Of Heath Stroke Scale) in the evaluation
neurological. By hard clinical differentiation with ischemic
stroke, a neuroimaging test for diagnostic confirmation of
HIP is essential14-16.
Complementary exams
In addition to a rapid clinical history and neurological
examination, computed tomography without hire (TCSC) of
the skull is highly sensitive and specific for hemorrhagic
stroke and is the key to early diagnosis17.
In the HIP, it will reveal not only the location and size of the
hemorrhage but also the intraventricular extension, the
mass effect, the hydrocephalus and the first signs of
herniation. The volume of the hematoma can be estimated
using the ABC/2 method, where6-9,18:
A - Is the maximum diameter of the hematoma (in cm);
B - Is the largest perpendicular diameter A (in cm);
C - Is the sum of the points obtained with the 10mm
cuts, in which the main axis of the hematoma presents:
75% to 100% of a = 1 point for each cut;
25% to 50% of a = 0.5 point each cut;
≤ 25% of a = Do not score;
Hematoma Volume (mL) = A x B x C / 2
This calculation of the hematoma volume, although variable
among the examiners, proved to be sufficient for clinical
decision making since hematomas with more than 30mL
have a worse prognosis.
MRI can be as sensitive as CCTSC to determine the presence
of hemorrhage, but rarely offers additional information in
the acute situation, and may be performed when there is
suspicion of non-hypertensive etiology (Cavernomas,
Angiopathy Amyloid, Neoplasms, among others). As a
general rule, the hyperacute hematoma is isointense in T1,
hyperintense in T2 and hypointense in T2. After the seventh
day, it becomes hyperintense on T1 and T2 due to
hemoglobin degradation in Methemoglobin, and in the
chronic phase, the low signal of hemosiderin is better
visualized in T2 or T219.
Angiography is indicated for investigation of secondary
causes such as AVM, aneurysms, fistulas, venous sinus
thrombosis and vasculitides in patients with atypical HIP
localization or aged below 45 years (regardless of the
presence of SAH). The method of choice is conventional
catheter angiography, butCT orMRI angiographywithuseof

Gadolinium are less invasive alternatives with good
sensitivity (Figure 1)12.
Figure1. The typical locations of hypertensive HIP are:
Putamen (A), thalamus (B), white matter Subcortical (C),
Bridge (D) and cerebellum (e). Thalamic hemorrhages and
Subcortical Frequently Extend to the ventricles (B and C).
ADrug search or vascular anomaly often causes bleeding
Lobar (F). Source: Dastur et al, 2017.
Prognosis
Despite the diagnostic and therapeutic advances, HIP
continues to present high Indices of mortality and disability.
The main factors related to the poor prognosis in the short
term (in 30 days) of these patients are initial volume of
hemorrhage more significant than 30cm³, lowering of the
level of consciousness at admission, intraventricular
bleeding, advanced age, and localization primarily
Infratentorial20.
For stratification of the risk of mortality in 30 days, the HIP
scale is the most used. Scores between0 and2 are associated
with low mortality and scores ≥ 3 are associated with a high
mortality rate (Table 1)7,11.
Table1. HIP Scale
Components Points
Glasgow Scale
3-4
5-12
13-15
2
1
0
Hematoma Volume (cm³)
≥ 30
< 30
1
0
Ventricular flooding
Yes
No
1
0
Origin Infratentorial
Yes
No
1
0
Age (years)
≥ 80
< 80
1
0
Total 0-6
Source: Hemphill et al. (2001)
Treatment
There is no specific treatment for the HIP. The initial
approach should be focused on airway evaluation,
respiratory and hemodynamic parameters, temperature,
capillary glycemia and detection of focal and external
neurological signs of trauma and its complications21.Airway
stabilization, respiration, and circulation (ABC)are essential
to prevent secondary injuries caused by hypoxemia,
uncontrolled hypertension, and hematoma expansion.
Intubation for airway protection isindicatedin patients with
Glasgow Scale (GCS) ≤8 or significant respiratory distress.
Ideally, after performing the neuroimaging exam, patients
with HIP should be quickly referred to beds monitored in a
stroke unit or intensive care beds10-13.
Temperature
Fever is an independent risk factor for poor prognosis. In
about 20% of patients, there is no infection and fever is
attributed to inflammatory responsestoextravasatedblood,
predominating in those with a poor clinical condition at
admission and in those with an intraventricular extension of
hemorrhage7-9. It is suggested that hyperthermia (axillary
temperature ≥37.5ºC) is treated in the acute phase of HIP
usually with acetaminophen ordipyrone.Inrefractorycases,
it may be associated with anti-inflammatory non-steroidal,
external physical methods and internal active cooling
(intravascular cooling catheters), although there are no
studies proving efficacy and safetyof coolingin patientswith
hemorrhagic stroke1-3.
Glucose
Care should be taken to avoid hyperglycemia and
hypoglycemia. Insulin therapy is recommended in order to
reach blood glucose levels between 100-140mg/dL For
patients with hemorrhagic stroke16,17.
Prophylaxis for venous thromboembolism (VTE)
There is a significant risk of VTE in patients with
hemorrhagic stroke. Therefore, in patients with HIP
restricted to bed, it is recommended to start the mechanical
prophylaxis of VTE, preferably with intermittent pneumatic
compression devices, or if not available, compression
stockings graduated at the time of admission. Associated
with mechanical prophylaxis, the prophylactic dosesof non-
fractioned subcutaneous heparin or LMWH may be initiated
after the first 48h in patients with documented stable
hematoma22,23.
Blood pressure (BP)
In the HIP, the elevation of systolic blood pressure (SBP) is
associated with the expansion of thehematoma,neurological
deterioration, and lower prognosis. Thus, treatment is
suggested if SBP>180mmHg and mean BP (map) >
130mmHg, aiming to reach a BP close to 160x90mmHg (or
Pam <110 mmHg)18-20. In patients with intracranial
hypertension,SBP should bemaintained above90mmHg and
ideally, intracranial pressure (PIC) monitoring should be
used to maintain cerebral perfusion pressure (CPP) above
60–80mmHg (PPC = PAM – PIC)6.
The medications antihypertensive generally used in the
acute phase of the HIP are Metoprolol, Diltiazem or Esmolol
since the Labetalol And Nicardipine are not available for use
in Brazil (Table 3). For more severe or refractory cases, it is
recommended to Nitroprusside of sodium IV, paying
attention to a potential increase in ICP. Oral anti-
hypertensive medicinal products should be instituted as
soon as possible (Tables 2 - 3)1.

Table2. Blood pressure control in HIP
Blood pressure Conduct
SBP >200 mmHg or
PAM>150 mmHg (two
readings with a 5-
minute interval)
Initiate aggressive BP
reduction by continuous
infusion of intravenous
antihypertensive medication
with BP monitoring every 5
minutes.
PAS>180 mmHg or
PAM>130mmHg
Suspected increase in
ICP
Consider ICP monitoring.
Initiate BP reduction by
continuous or intermittent
infusion of intravenous
antihypertensive medication
with BP monitoring every 5
minutes. Keep PPC>60-
80mmHg.
PAS>180 mmHg or
PAM>130 mmHg
No suspected increase
in ICP
Initiate moderate BP reduction
by continuous or intermittent
infusion of antihypertensive
With BP monitoring every 15
minutes (target BP
160x90mmhg or PAM target
110mmhg).
PAS<90mmHg
Expansion with Crystalloids
intravenously and infusion of
vasoactive amines: Dopamine
2 – 20mg/Kg/min. /
noradrenaline 0.05 – 0.2
mg/Kg/min.
BP: blood pressure; PAM: mean arterial pressure; ICP:
Intracranial pressure; PPC: Cerebral perfusion pressure
source: Pontes-Neto et al. (2009).
Table3. Antihypertensive medications used in HIP
Drug
Intravenous
Dose
Contraindications
Metoprolol
5mg-1ML/min
every 10 min, up
to a maximum of
20 min.
Severe HF, COPD,
asthma,
hypotension,
bradycardia
Enalapril
0,625-1.25 mg in
5min every 6h.
Sudden BP drop in
renin-increasing
states. ARF if renal
artery stenosis.
Diltiazen
0.25-0.35mg/kg
at 10min
Infusion 5-15
mg/h.
Sinus node disease
or atrioventricular
node. Severe HF
Nitroprusside
Sodium
0.25-10
mg/Kg/min.
Potential increase
in ICP, variable
response, cyanide
poisoning and
Thiocyanate.
Esmolol
250-
500mg/Kg/min
in bolus every
10min or
infusion 25-
300mg/Kg/min
Severe HF, COPD,
asthma,
hypotension,
bradycardia.
HF: Heart failure; ARF: acute renal failure; COPD:
Chronic obstructive pulmonary disease; BP: blood
pressure;ICP:Intracranialpressure.Source:Modifiedde
Pontes-Neto et al. (2009)
Intracranial hypertension
Increased intracranial pressure (ICP/PIC) due to HIP may
result from the hematoma itself and the surroundingedema,
which may contribute to brain injury and neurological
deterioration. A graded approach is recommended starting
with simple measures that include7-9:
Elevation of the headboard in 30⁰ and positioning of the
head, avoiding excessive flexion or rotation of the neck;
Analgesia (Morphine or Fentanyl) and Sedation
(Propofol, Etomidate Or Midazolam) particularly in
unstable and intubated patients;
Keep the Euvolemia: If necessary, isotonic fluids (e.g.,
saline solution 0.9%) should be administered.
BP control;
Treatment of fever and seizures;
Invasive monitoring and specific treatment of PIC should be
considered for patients with GCS<8, with clinical evidence of
herniation transtentorial or with significantintraventricular
hemorrhage or hydrocephalus12. The goal should be to keep
the PIC< 20mmHg. More aggressive therapies to obtain this
control include osmotic diuretics (e.g., mannitol and
hypertonic saline solution), neuromuscular blockade,
hyperventilation, hypothermia, and Ventriculostomy 10,13-15.
Mannitol 20%: bolus Initial dose of 1g/Kg, followed by
infusions from 0.25 to 0.5 g/Kg/dose (IV) administered
for 20min, from 6/6 hours (usual maximum dosage: 2
g/Kg);
Hypertonic Saline Solution: NaCl 3%, in continuous
infusion, with control of serum sodium every 6h,
respecting the maximum increase of sodium around 15
mEq/L/day, in refractory cases;
Analgesia and/or neuromuscular blockade:
barbiturates (phenobarbital 5-20 mg/Hg in bolus
followed by 1-4mg/Kg/h) associated or not with non-
depolarizing neuromuscular blockers;
Hyperventilation: The objective is to reduce the PaC02
to levels between 25-30 mmHg, determining almost
immediate cerebral vasoconstriction. It causes a
reduction of 25%-30% in intracranial pressure, with
maximum effect in approximately thirty minutes.
Induced hypothermia: through the cooling of all the
body, its objective is to maintain a temperature of 32-
34oC, but its therapeutic use in the elevated PIC remains
controversial and should be limited to refractory
patients.
Ventriculostomy: indicated in obstructive
hydrocephalus (a common complication of thalamic
hemorrhage with compression of the III ventricle and
cerebellar hemorrhage with compression of the IV
ventricle) or intraventricular hemorrhage with
hydrocephalus.
Reversal of Coagulopathies
Approximately 12-20% of patientswithHIP makeuseof oral
anticoagulants. In this way, the rapid correction of the
coagulopathy should be considered in any potentially
recoverable patient, and any antithromboticagentshould be
discontinued immediately. The method of reversal will
depend on the agent used and should not be postponeduntil
the results of the laboratory coagulationtestshavearrived24.
If you use warfarin: immediately administer fresh frozen
plasma (FFP) or complex concentrate Prothrombin (CCP)
and vitamin K (IV) 10mg until normalizationof prothrombin
time measured by means of INR<1.4. CCP is an inactivated

concentrate of factors II, IX and X, with variable amounts of
factor VII, its concentration of coagulationfactorsdependent
on vitamin K is about 25 times greater than that of fresh
frozen plasma (FFP) and can reverse the coagulopathy
rapidly, with lower volume and lower risk of infection,
pulmonary edema, transfusion-related acute lung injury
(Trali) and cardiac overload associated with transfusion
(COAT)9-11.
If the use of unfractionated heparin: administer sulfate
Protamine (IV) 1mg for each 100units of heparin
administered in the last 2-3 hours (maximum50mg).Repeat
half of the initial dose if ttpa remains elevated3.
If symptomatic HIP associated withtheuseof thrombolytics:
administer fresh frozen plasma, cryoprecipitate, and
platelets18.
Seizures
HIP patient has up to 16% risk of clinical seizures within a
week, Particularly In thosewherethereishemorrhageLobar
With intraventricular flooding. Therefore, prophylactic
treatment with anticonvulsants is recommended in patients
with torporous and comatose with activity Epileptiform
Electroencephalogram(EEG)inpatientswith bleedingLobar
and in those where there are signs of intracranial
hypertension25. The drugs of choice are Phenytoin and
Phenobarbital, which should be maintained at therapeutic
serum levels for one month and subsequently withdrawn
gradually14.
Surgery
Surgical interventions to approach the mass effect by the
hematoma include Craniotomy Decompressive of the
posterior fossa or drainage of the hematoma and are
indications6,18:
Cerebellar Hematoma >3cm in diameter with
deterioration brain stem compression and/or
hydrocephalus;
Bleeding Lobar voluminous and in up to 1cm from the
surface of the cerebral cortex, especially in young
patients, with scores on the Glasgow coma scale
between nine and twelve.
In cases of hydrocephalus, an external ventricularshuntmay
be necessary during the critical period of ICP elevation26.
The Craniotomy Is the most studied surgical technique in
patients with HIP supratentorial. However, other methods
include endoscopicaspirationofthehemorrhage, fibrinolytic
therapy to undo the clot followed by aspiration and
aspiration stereotactic guided by CT. Studies of these less
invasive techniques are underway27,28.
Conclusion
The acute treatment of intraparenchymal cerebral
hemorrhage is still a subject that remains in an intense
investigation. The lack of guidelines and more current
guidelines in Brazil evidences the need for scientificreviews
with explicit language, which seek to standardize care and
practical approach to patients who are affected by this
disease.
Although there is no consensus yet, the multiple ongoing
studies show evidence of efficacy in reducingbloodpressure
and redefining new targets. Recent neuroimaging studies
already reveal patterns that identify patients who benefit
most from minimally invasive surgeries. And
neuroprotection studies in surrounding areas of the lesion
confirm the benefit of correct measures of intracranial
hypertension, glycemic control, and body temperature.
The treatment of intracranial hemorrhage continues to be
directed towards the reduction of disability and morbidity
and mortality. However, prevention measures are widely
studied and disseminated in clinical practice. In this area of
prevention, adequateblood pressurecontrolis of paramount
importance.
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